2. Five air pollutants are responsible
for 98% of air pollution:
• CO or carbon monoxide (52%)
• sulfur oxides (14%)
• hydrocarbons (14%)
• nitrogen oxides (14%)
• different particles (4%)
Main air pollutants
4. Diseases caused by air
pollutants
• bronchitis
• ventilatory obstructive diseases
• pulmonary emphysema
• bronhcial asthma
• lung cancer
5. Carbon monoxide (CO)
CO is non irritating gas
without color, taste and smell.
It is incomplete combustion
byproduct.
6. Carbon monoxide (CO)
• Average concentration in atmosphere
is 0,1 ppm, but in dense traffic
conditions concentration can be even
more than 100 ppm.
• Treshold limit values (TLV) during 8
hours working day (40 hours working
week) is 25 ppm.
7. Action mechanism
• CO competes reversibly for oxygen
binding sites on hemoglobin.
• CO has 220 times higher affinity
than oxygen.
• Carboxyhemoglobin can not
transport oxygen.
8. Action mechanism
• Carboxyhemoglobin interferes
with oxygen dissociation from
remaining oxyhemoglobin.
• The most affected tissues are
BRAIN and HEART.
9. Action mechanism
• Healthy non smoker has levels of
carboxyhemoglobin lower than 1% of
overall hemoglobin.
• For smokers that level is 5-10%.
• For person breathing polluted air with
levels of 1000 pm CO, there is 50%
of carboxygemoglobin.
11. Clinical effects
Levels of
carboxyhemoglobin
Symptoms
<15% Headache, depression
25% Headache, fatigue, reduced attention,
loss of fine motoric coordination
40% Syncope, collapse
>60% Death can occur because of irreversible
myocardial and brain damage.
12. Clinical effects
• Clinical symptoms worsen during
hard physical work, on great altitudes
and high ambient temperatures.
• Chronic exposure to low levels of CO
(like in smokers) induce
atherosclerotic coronary arteries
disease.
13. Treatment
1. Relocate a person from a source of
poisoning!
2. Maintenance of normal breathing!
3. Oxygen!
4. Hyperbaric chamber in severe poisoning!
14. Treatment
Half time elimination of CO in
ambient of 1 atm is 320 min.
With 100% oxygen half time
elimination is 80 minutes.
With hyperbaric oxygen (2-3 atm)
half time is 20 minutes.
16. Action mechanism
• In contact with wet membranes,
SO2 creates sulfuric acid with
irritating effect on eyes, mucosa
and skin.
• 90% of inhaled SO2 absorbes in
upper respiratory tract where it
causes bronchoconstriction.
17. Action mechanism
Levels of 5-10 ppm cause
severe bronhcospasm.
Patients with asthma are
more susceptible on SO2.
18. Clinical presentation
• Irritation of eyes, nose and throat.
• Reflex bronchoconstriction.
• Status asthmaticus in patients with
asthma.
• Delayed pulmonary oedema in
cases of severe poisoning.
19. Clinical presentation
• In cases of chronic exposure
there may be worsening of
chronic cardiopulmonal
disease.
• There is no specific
treatment/antidote.
20. Nitrogen dioxide
• NO2 is brownish irritating gas
that can sometimes be
associated with fire.
• It is produced in silos and can
cause SILO FILLER´S DISEASE
in silo workers.
21. Action mechanism
• NO2 is relatively insoluble gas that
can cause pulmonary oedema.
• In acute exposure alveolar cells
type 1 are damaged.
• In higher levels exposure both type
1 and 2 alveolar cells can be
damaged.
22. Action mechanism
• Exposure to 50 ppm levels of NO2
during 1 hour can cause pulmonary
oedema.
• Subacute and chronic pulmonary
lesions can also occur.
• Levels of 100 ppm can cause severe
pulmonary oedema and death.
24. Clinical presentation
• Pulmonary oedema develops after 1
to 2 hours of exposure.
• In some patients after 2 weeks there
can be a second fase of disease
worsening with repeated pulmonary
oedema and bronchiolitis obliterans.
• There is no specific antidote.
25. Ozone (O3)
• O3 causes mucosa irritation.
• Mild exposure causes irritation of
upper respiratory tract.
• Severe exposure causes deep
pulmonary irritation with
pulmonary oedema.
26. Ozone (O3)
• Ozone causes shallow and
fast breathing, and decrease
of pulmonary compliance.
• Pulmonary damage occurs at
levels higher than 0,8 ppm.
27. Ozone (O3)
• Chronic exposure can cause
chronic bronchitis,
bronchiolitis, fibrosis and
pulmonary emphysema
(concentrations >1 ppm).
• There is no specific antidote.
